TB Knee

Tuberculous arthritis of the knee is the most common peripheral joint TB after the hip. The knee, being a large synovial joint with abundant synovial tissue and relatively superficial anatomy, is vulnerable to haematogenous TB seeding. The presentation is typically subacute or chronic, and the diagnosis is often delayed because the differential diagnosis is broad and TB is not always the first consideration in non-endemic settings.

• The knee accounts for approximately 10–15% of osteoarticular TB cases; second most common peripheral joint involved after the hip
• Demographics: any age; children and young adults in endemic regions; elderly and immunocompromised in developed countries
• Pathogenesis: haematogenous seeding → synovial granulomatous inflammation → progressive cartilage and bone destruction; the abundant synovial tissue of the knee makes synovitis the dominant early feature
• Average delay to diagnosis in TB knee: 12–18 months in most series — the insidious onset, low-grade nature, and broad differential diagnosis (RA, pigmented villonodular synovitis, chronic synovitis) frequently leads to missed or delayed diagnosis; always consider TB in any chronic monoarthritis
• Co-existing pulmonary TB in approximately 40–50% — investigate in all suspected cases

• Phemister triad applies equally to TB knee: periarticular osteoporosis + marginal erosions + gradual (not rapid) joint space narrowing; the gradual narrowing differentiates TB from pyogenic arthritis (rapid) and from osteoarthritis (asymmetric, osteophytes present)
• Unlike OA or pyogenic arthritis, TB initially spares cartilage — early stages show periarticular osteoporosis before cartilage loss begins; this is an important distinguishing feature

• Gradual onset of knee pain, swelling, and limp over weeks to months; low-grade fever; night sweats and weight loss may be present
• Physical examination: warm, swollen, tender knee; restricted range of motion (flexion contracture develops early); quadriceps wasting (marked, early); effusion; doughy soft tissue consistency from synovial thickening
• Quadriceps wasting out of proportion to clinical symptoms — a classic feature of TB knee; rapid and prominent muscle wasting occurs early, often before significant joint destruction, from neurogenic inhibition and disuse
• Cold abscess: may present as a popliteal swelling tracking through the posterior capsule, or along the medial or lateral soft tissues; non-tender, fluctuant
• Sinus tracts: in neglected cases; discharging thin, watery material; secondary bacterial infection worsens prognosis
• Children: painful limping; irritable knee; distinguishable from septic arthritis by insidious onset and less severe systemic illness; Mantoux positive

• Plain radiographs: AP and lateral weight-bearing films; Phemister triad; assess for bony destruction and deformity
• MRI knee: best for early diagnosis — synovial thickening and enhancement (pannus), bone marrow oedema, marginal erosions, subchondral changes, abscess formation; distinguishes from other causes of synovitis
• Joint aspiration: turbid or clear fluid; sent for AFB smear (positive in approximately 20%), TB culture (positive in 50–60%), and PCR (rapid, sensitive); cells predominantly lymphocytes (unlike pyogenic where PMNs predominate); send for AFB AND standard culture — secondary bacterial infection possible
• Synovial biopsy: definitive diagnostic test — open or arthroscopic; caseating epithelioid granulomas with Langhans giant cells; AFB culture of tissue (up to 90% sensitivity)
• IGRA / Mantoux: supports diagnosis but does not confirm active disease
• Chest X-ray: active or healed pulmonary TB; CT chest if CXR equivocal
• Bloods: ESR and CRP elevated; WBC often normal; lymphocyte predominance

• PVNS vs TB knee: both present with chronic monoarthritis and synovial proliferation; PVNS has characteristic haemosiderin-staining on MRI (blooming on T2*); biopsy distinguishes them definitively; do not treat TB knee with corticosteroids (given to PVNS) — will worsen TB dramatically

• RIPE anti-tuberculous chemotherapy: same standard regimen as hip TB — rifampicin, isoniazid, pyrazinamide, ethambutol × 2 months intensive phase; then rifampicin + isoniazid × 4 months continuation; minimum 6 months total; most guidelines recommend 9–12 months for skeletal TB
• Adjunctive corticosteroids: may reduce synovial inflammation and prevent adhesion formation in early synovitic stage; used under cover of anti-TB chemotherapy; not given without concurrent anti-TB therapy
• Splintage and protected weight-bearing: reduce pain and prevent deformity during treatment; progressive rehabilitation as inflammation resolves
• Medical treatment alone is curative for Stage I–II disease in most patients when initiated early and completed fully

• TKA in healed TB knee: evidence shows safe and effective results with low reactivation rates (2–5%) when anti-TB chemotherapy is maintained perioperatively; constrained or hinged implants may be required if ligamentous integrity is compromised by prior disease; pre-operative MRI to assess bone stock and ligament integrity
• Sinus tract excision: any communicating sinus tracts must be excised and allowed to heal before TKA to reduce infection risk — stage the procedure if sinus tracts present

• Corticosteroids in TB knee — extreme caution: adjuvant steroids are occasionally used in the synovitic stage with concurrent anti-TB therapy to reduce inflammation; however, inadvertent steroid use in undiagnosed TB knee (e.g., treating as inflammatory arthritis) causes rapid disease acceleration and dissemination — a diagnostic pitfall that must be avoided; always confirm diagnosis before steroid administration
• TKA implant selection in TB knee: posterior-stabilised (PS) implants preferred when PCL is destroyed; constrained condylar (CCK) or hinged implant for collateral ligament deficiency from severe bone destruction; pre-operative assessment of ligament status with stress X-rays and examination under anaesthesia guides selection
• Arthrodesis vs TKA for young TB knee: arthrodesis provides durable, reliable, pain-free function without infection risk; gait is abnormal (stiff leg) but functional; TKA provides better functional outcomes but carries small reactivation risk; patient preference, activity level, and bilateral involvement should guide choice
• Bilateral TB knee: uncommon; requires sequential TKA under continuous anti-TB cover; arthrodesis bilaterally is not feasible (patient would be unable to sit); TKA preferred bilaterally
• MDR-TB knee: requires specialist input; second-line agents; surgery may be needed for diagnostic or therapeutic purposes; prosthetic surgery should be avoided until drug sensitivity confirmed and effective regimen established

• Phemister triad: periarticular osteoporosis + marginal erosions + gradual joint space narrowing — TB knee; distinguish from rapid destruction (pyogenic) and osteophytes (OA)
• Quadriceps wasting out of proportion to symptoms — classic early clinical feature of TB knee
• Diagnostic delay of 12–18 months is typical — always consider TB in any chronic monoarthritis, especially in endemic regions or immunocompromised patients
• Synovial biopsy: caseating granulomas + Langhans giant cells; tissue culture 90% sensitive
• Joint fluid: lymphocyte predominance (vs PMN in pyogenic); AFB smear only 20% positive; culture 50–60%
• PVNS vs TB knee: MRI distinguishes — haemosiderin blooming on T2* = PVNS; biopsy confirms; do not give steroids without TB excluded
• RIPE × 9–12 months for skeletal TB; minimum 2–3 months before elective TKA
• TKA in healed TB: safe; reactivation 2–5%; continue anti-TB for 6 months post-TKA; PS or constrained implant based on ligament integrity
• Arthrodesis: preferred in young, heavy, manual worker with Stage IV disease — avoids prosthetic reactivation risk
• Steroids without anti-TB cover: catastrophic — rapid dissemination and disease acceleration; never give until TB excluded